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Medical and surgical emergencies
Advanced cardiac life support (ACLS): Clinical (To be retired)
Supraventricular arrhythmias: Pathology review
Ventricular arrhythmias: Pathology review
Heart blocks: Pathology review
Coronary artery disease: Clinical (To be retired)
Heart failure: Clinical (To be retired)
Syncope: Clinical (To be retired)
Pericardial disease: Clinical (To be retired)
Valvular heart disease: Clinical (To be retired)
Chest trauma: Clinical (To be retired)
Shock: Clinical (To be retired)
Peripheral vascular disease: Clinical (To be retired)
Leg ulcers: Clinical (To be retired)
Aortic aneurysms and dissections: Clinical (To be retired)
Cholinomimetics: Direct agonists
Cholinomimetics: Indirect agonists (anticholinesterases)
Muscarinic antagonists
Sympathomimetics: Direct agonists
Sympatholytics: Alpha-2 agonists
Adrenergic antagonists: Presynaptic
Adrenergic antagonists: Alpha blockers
Adrenergic antagonists: Beta blockers
ACE inhibitors, ARBs and direct renin inhibitors
Loop diuretics
Thiazide and thiazide-like diuretics
Calcium channel blockers
cGMP mediated smooth muscle vasodilators
Class I antiarrhythmics: Sodium channel blockers
Class II antiarrhythmics: Beta blockers
Class III antiarrhythmics: Potassium channel blockers
Class IV antiarrhythmics: Calcium channel blockers and others
Positive inotropic medications
Antiplatelet medications
Blistering skin disorders: Clinical (To be retired)
Bites and stings: Clinical (To be retired)
Burns: Clinical (To be retired)
Diabetes mellitus: Clinical (To be retired)
Hyperthyroidism: Clinical (To be retired)
Hypothyroidism and thyroiditis: Clinical (To be retired)
Parathyroid conditions and calcium imbalance: Clinical (To be retired)
Adrenal insufficiency: Clinical (To be retired)
Neck trauma: Clinical (To be retired)
Insulins
Mineralocorticoids and mineralocorticoid antagonists
Glucocorticoids
Abdominal pain: Clinical (To be retired)
Appendicitis: Clinical (To be retired)
Gastrointestinal bleeding: Clinical (To be retired)
Peptic ulcers and stomach cancer: Clinical (To be retired)
Inflammatory bowel disease: Clinical (To be retired)
Diverticular disease: Clinical (To be retired)
Gallbladder disorders: Clinical (To be retired)
Pancreatitis: Clinical (To be retired)
Cirrhosis: Clinical (To be retired)
Hernias: Clinical (To be retired)
Bowel obstruction: Clinical (To be retired)
Abdominal trauma: Clinical (To be retired)
Laxatives and cathartics
Antidiarrheals
Acid reducing medications
Blood products and transfusion: Clinical (To be retired)
Venous thromboembolism: Clinical (To be retired)
Anticoagulants: Heparin
Anticoagulants: Warfarin
Anticoagulants: Direct factor inhibitors
Antiplatelet medications
Thrombolytics
Fever of unknown origin: Clinical (To be retired)
Infective endocarditis: Clinical (To be retired)
Pneumonia: Clinical (To be retired)
Tuberculosis: Pathology review
Diarrhea: Clinical (To be retired)
Urinary tract infections: Clinical (To be retired)
Meningitis, encephalitis and brain abscesses: Clinical (To be retired)
Bites and stings: Clinical (To be retired)
Skin and soft tissue infections: Clinical (To be retired)
Protein synthesis inhibitors: Aminoglycosides
Antimetabolites: Sulfonamides and trimethoprim
Antituberculosis medications
Miscellaneous cell wall synthesis inhibitors
Protein synthesis inhibitors: Tetracyclines
Cell wall synthesis inhibitors: Penicillins
Miscellaneous protein synthesis inhibitors
Cell wall synthesis inhibitors: Cephalosporins
DNA synthesis inhibitors: Metronidazole
DNA synthesis inhibitors: Fluoroquinolones
Herpesvirus medications
Azoles
Echinocandins
Miscellaneous antifungal medications
Anthelmintic medications
Antimalarials
Anti-mite and louse medications
Hypernatremia: Clinical (To be retired)
Hyponatremia: Clinical (To be retired)
Hyperkalemia: Clinical (To be retired)
Hypokalemia: Clinical (To be retired)
Metabolic and respiratory acidosis: Clinical (To be retired)
Metabolic and respiratory alkalosis: Clinical (To be retired)
Toxidromes: Clinical (To be retired)
Medication overdoses and toxicities: Pathology review
Environmental and chemical toxicities: Pathology review
Acute kidney injury: Clinical (To be retired)
Kidney stones: Clinical (To be retired)
Adrenergic antagonists: Alpha blockers
Stroke: Clinical (To be retired)
Seizures: Clinical (To be retired)
Headaches: Clinical (To be retired)
Traumatic brain injury: Clinical (To be retired)
Neck trauma: Clinical (To be retired)
Lower back pain: Clinical (To be retired)
Spinal cord disorders: Pathology review
Anticonvulsants and anxiolytics: Barbiturates
Anticonvulsants and anxiolytics: Benzodiazepines
Nonbenzodiazepine anticonvulsants
Migraine medications
Osmotic diuretics
Antiplatelet medications
Thrombolytics
Opioid agonists, mixed agonist-antagonists and partial agonists
Opioid antagonists
Asthma: Clinical (To be retired)
Chronic obstructive pulmonary disease (COPD): Clinical (To be retired)
Venous thromboembolism: Clinical (To be retired)
Acute respiratory distress syndrome: Clinical (To be retired)
Pleural effusion: Clinical (To be retired)
Pneumothorax: Clinical (To be retired)
Chest trauma: Clinical (To be retired)
Bronchodilators: Beta 2-agonists and muscarinic antagonists
Pulmonary corticosteroids and mast cell inhibitors
Joint pain: Clinical (To be retired)
Anatomy clinical correlates: Clavicle and shoulder
Anatomy clinical correlates: Axilla
Anatomy clinical correlates: Arm, elbow and forearm
Anatomy clinical correlates: Wrist and hand
Anatomy clinical correlates: Median, ulnar and radial nerves
Anatomy clinical correlates: Bones, joints and muscles of the back
Anatomy clinical correlates: Hip, gluteal region and thigh
Anatomy clinical correlates: Knee
Anatomy clinical correlates: Leg and ankle
Anatomy clinical correlates: Foot
Acetaminophen (Paracetamol)
Non-steroidal anti-inflammatory drugs
Glucocorticoids
Opioid agonists, mixed agonist-antagonists and partial agonists
Antigout medications
Venous thromboembolism: Clinical (To be retired)
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Our bodies are constantly maintaining a fine balance between making and breaking blood clots. In the late 1800s, doctor Rudolf Virchow identified three factors that contribute towards the formation of clots: hypercoagulability, stasis of the blood, and endothelial injury. If there’s any factor that tips the balance towards forming clots then a venous thromboembolism, or VTE can develop. VTE can cause two clinical presentations: deep vein thrombosis, or DVT, and pulmonary embolism, or PE. They are clumped together because they share the same pathophysiology, and often a DVT leads to a PE.
Risk factors for VTE revolve around Virchow’s triad, and can be remembered with the mnemonic “THROMBOSIS”: “T” is for trauma or history of travel. “H” is for hospitalization and hormones, meaning any form of exogenous estrogen such as hormone replacement therapy, tamoxifen or combined oral contraceptives, which promote the formation of clots in the venous circulation. “R” is for relatives, that is family history of inherited hypercoagulable disorders, like Factor V Leiden. “O” is for old age. “M” is for having any malignancy. “B” is for long bone fractures. “O” is for obesity and obstetrics; that is pregnancy and the early post-partum period. “S” is for any form of major surgery, especially orthopedic surgery as well as smoking. “I” is for immobilization, such as a paralyzed limb. And the final “S” is for other sickness, like antiphospholipid syndrome, nephrotic syndrome, and paroxysmal nocturnal hemoglobinuria.
Alright, now DVTs usually involve the deep veins of the lower extremity, such as the proximal iliac and femoral veins, or the distal popliteal veins. Upper extremity DVTs are very rare, and if they do happen, it’s usually because of an indwelling intravascular catheter. Now, individuals with DVT usually develop a swollen, red and painful unilateral limb. That sounds nonspecific, so it’s important to differentiate DVT from superficial thrombophlebitis, cellulitis, lymphedema, and Baker cysts. On physical exam, a great telltale sign of DVT is a large calf diameter relative to the unaffected leg. A commonly taught finding is the Homan’s sign; which is calf pain on passive dorsiflexion of the foot, but this finding is unreliable. The rare but severe presentations of DVT have latin names - phlegmasia cerulea dolens, which translates to a painful blue swelling, and phlegmasia alba dolens, which translates to painful white swelling. Painful blue swelling can occur due to massive iliofemoral thrombosis, which causes severe venous congestion in the affected limb. Painful white swelling can occur due to a massive thrombosis that gets so big that it compresses nearby arteries, causing the leg to become pale due to arterial insufficiency and ischemia.
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